At a Glance

a tendency to hyponatremia and hypo-osmolality when fluid intake is excessively high

polyuria, with an appropriate hypo-osmolar urine

appropriate suppression of plasma vasopressin

fluid restriction restoring fluid balance

Primary polydipsia is a state of markedly increased fluid intake in the setting of a normal vasopressin system and normal renal tubular function.In primary polydipsia, urine osmolality increases in response to water deprivation (in some cases to >600 mosmol/kg H2O), and there would be no further response to injected desmopressin.

The hallmark of this condition is the consumption of copious volumes of liquid with an attendant polyuria. Electrolyte analysis may be entirely normal, but, with a very high volume of intake, usually exceeding 15-18 liters per day, the individual may suffer from hyponatremia and a low serum osmolality. Urine osmolality will be extremely low, typically less than 100 mosmols/kg H2O. (In diabetes insipidus, the serum, if anything, may show an increased osmolality). Urine osmolality will be entirely appropriate for the low serum osmolality.

The term “primary polydipsia” is often termed "psychogenic polydipsia." Others have classified primary polydipsia into dipsogenic (inappropriate thirst caused by a disturbed osmoreceptor mechanism), psychogenic (obsessive water consumption due to disordered thinking), or even iatrogenic (increased water drinking due to supposed health benefits). It is not clear that these subsets can really be distinguished, thus, primary polydipsia is preferred.

What Tests Should I Request to Confirm My Clinical Dx? In addition, what follow-up tests might be useful?

A 24-hour urine collection, performed as an outpatient, in which the individual has free access to fluids, will confirm the polyuria and the low urine osmolality. A plasma vasopressin will be appropriately suppressed (i.e., very low). Fluid restriction in a well-controlled environment will produce a rise in both serum and urine osmolality. At most, the serum osmolality would be expected to rise into the population reference range; the patient will not become hypernatremic or hyperosmolar. Plasma vasopressin will be expected to rise into the population reference range, and the concentration should be appropriate for the plasma osmolality. Urine concentration will increase with water restriction. This increase may be significant, but may be modest, since prolonged polydipsia "washes out" the renal inner medullary urea gradient and prolonged suppression of vasopressin decreases aquaporin expression in collecting duct cells.

An injection of synthetic vasopressin will not elicit a change in serum and urine osmolality, since secretion of endogenous vasopressin is normal and appropriate. (Table 1)

Table 1.

Test Results Indicative of the Disorder

Initial Urine osmolality (mosmols/kg H2O)

H2O Deprivation Test

Desmopressin Injection

>300 - solute diuresis (e.g., diabetes mellitus)

In primary polydipsia, urine osmolality increases with water restriction so that urine-to-plasma osmolality exceeds 1.0.

There is no significant response to exogenous desmopressin in primary polydipsia.

Are There Any Factors That Might Affect the Lab Results? In particular, does your patient take any medications - OTC drugs or Herbals - that might affect the lab results?

Certain drugs that produce a dry mouth (xerostomia) may play a role in stimulating thirst. Antipsychotic, antidepressant, and anxiolytic agents are well-known causes of xerostomia.

What Lab Results Are Absolutely Confirmatory?

The key to the diagnosis is the response of the polyuria and urine osmolality to fluid restriction. A decrease in urine volume of rising osmolality signals that the homeostatic controls of water balance are functioning normally. This is especially so if the urine osmolality exceeds 600 mosmols/kg H2O.

What Confirmatory Tests Should I Request for My Clinical Dx? In addition, what follow-up tests might be useful?

If a patient has partial or incomplete central diabetes insipidus or partial nephrogenic diabetes insipidus, fluid deprivation might result in a modest concentration of the urine, producing an effect similar to that encountered in primary polydipsia. Responses of urine osmolality to injected desmopressin may not be helpful because of overlap in the range of the responses. In this instance, there is utility in enhancing the serum osmolality by infusing hypertonic saline during the fluid restriction until the osmolality rises to greater than 300 mosmol/kg H2O. The volume loss combined with hyperosmolality will further stimulate vasopressin secretion in a normal individual. Determination of plasma vasopressin as a function of serum osmolality can better distinguish partial diabetes insipidus (DI) states and primary polydipsia.